Congestive heart failure affects an estimated 5 million people and results in an estimated $28.8 billion dollars being spent on health care relating to congestive heart failure (see AHA, 2003). As a result congestive heart failure treatments have become a substantial research interest.
There are numerous cardiac devices, artificial hearts and heart assist devices currently on the market. In addition, other therapies like drugs, biventricular pacing, stem cell therapies, blood contacting assist devices, surgical manipulations, or passive stents and constraints typically off-load the heart and thus only modulate the strain pattern indirectly (e.g., through greater ejection fraction).
Pharmacotherapy is minimally invasive and is a preferred form of treatment for congestive heart failure; however, pharmacotherapy has risks. Additionally, pharmacotherapy can be ineffective for mechanical problems, such that surgical intervention is necessary. For example, cardiovascular diseases with aberrant growth and remodeling may be in the class of diseases with a mechanical etiology, because it is now evident that local mechanical stimuli are major controllers of growth and remodeling in cardiovascular tissues. As the heart functions to produce mechanical work, mechanical strain may be one of the primary stimuli in cardiac development and adaptation.
For example, a recent publication (Rose et al., 2001) examined the Randomized Evaluation of Mechanical Assistance for the Treatment (“REMATCH trial”) of congestive heart failure (“CHF”). The REMATCH trial was a major, multi-center (20), large trial (129 patients) designed to compare long-term cardiac assist treatments to pharmacological treatment in the areas of survival, serious adverse events, number of days of hospitalization and quality of life. The REMATCH trial states, “Patients with mild-to-moderate heart failure [SOLVD, 1991] and, recently, some with more severe disease [Packer et al., 2001] have been shown to benefit from drug therapy. Nevertheless, the survival and the quality of life of patients with severe heart failure remain limited. Cardiac transplantation is the only treatment that provides substantial individual benefit, but with fewer than 3,000 donor hearts available worldwide per year, its impact is epidemiologically trivial [Hosenpud et al., 2000].”
Despite having an increased number of adverse events and hospitalizations, the group with mechanical assist had a significantly higher survival rate and quality of life. The success of the REMATCH trial contributed to the recent action of the FDA to approve cardiac assist devices for use in end-stage heart failure patients who are not waiting for a transplant. Prior to this, cardiac assist devices were only approved as a bridge to transplantation.
One heart assist device is shown in U.S. Pat. No. 5,119,804, issued on Jun. 9, 1992 to Anstadt, for a cardiac massage apparatus and a drive system. The cardiac massage apparatus includes a cup having a liner that is connected within the cup at its upper and lower ends. Dimensions defining an optimum cup shape as a function of ventricular length are disclosed wherein the heart remains within the cup when mechanically activated.
Other examples include U.S. Pat. Nos. 6,663,558; 6,612,979; 6,612,978; 6,602,184 and 6,595,912 issued to Lau, et al., for a cardiac harness to treat congestive heart failure. The harness applies elastic, compressive reinforcement on the left ventricle to reduce deleterious wall tension and to resist shape change of the ventricle during the mechanical cardiac cycle. Rather than imposing a dimension beyond which the heart cannot expand, the harness provides no hard limit over the range of diastolic expansion of the ventricle. Instead, the harness follows the contour of the heart throughout diastole and continuously exerts gentle resistance to stretch.
U.S. Pat. No. 6,602,182, issued Aug. 5, 2003 to Milbocker, for a unified, non-blood contacting, implantable heart assist system surrounds the natural heart and provides circumferential contraction in synchrony with the heart's natural contractions. The pumping unit includes adjacent tube pairs arranged along a bias with respect to the axis of the heart and bound in a non-distensible sheath forming a heart wrap. The tube pairs are tapered at both ends such that when they are juxtaposed and deflated they approximately follow the surface of the diastolic myocardium. Inflation of the tube pairs causes the wrap to follow the motion of the myocardial surface during systole. A muscle-driven or electromagnetically powered energy converter inflates the tubes using hydraulic fluid pressure. An implanted electronic controller detects electrical activity in the natural heart, synchronizes pumping activity with this signal, and measures and diagnoses system as well as physiological operating parameters for automated operation. A transcutaneous energy transmission and telemetry subsystem allows the Unified System to be controlled and powered externally.
U.S. Pat. No. 6,592,619, issued on Jul. 15, 2003 to Melvin, for an actuation system for assisting the operation of the natural heart. The system includes a framework for interfacing with a natural heart, through the wall of the heart, which includes an internal framework element configured to be positioned within the interior volume of a heart and an external framework element configured to be positioned proximate an exterior surface of the heart. The internal framework is flexibly suspended with respect to the external frame. An actuator system is coupled to the framework and configured to engage an exterior surface of the heart. The actuator system includes an actuator band extending along a portion of a heart wall exterior surface. The actuator band is selectively movable between an actuated state and a relaxed state and is operable, when in the actuated state, to assume a predetermined shape and thereby indent a portion of the heart wall to affect a reduction in the volume of the heart. A drive apparatus is coupled to the actuator band and is operable for selectively moving the actuator band between the relaxed and actuated states to achieve the desired assistance of the natural heart.
U.S. Pat. No. 6,224,540 issued on May 1, 2001 to Lederman, et al., relates to a passive girdle for heart ventricle for therapeutic aid to patients having ventricular dilatation. A passive girdle is wrapped around a heart muscle which has dilatation of a ventricle to conform to the size and shape of the heart and to constrain the dilatation during diastole. The girdle is formed of a material and structure that does not expand away from the heart but may, over an extended period of time be decreased in size as dilatation decreases.
Other heart assist devices include direct cardiac compression devices; however, these devices were designed to enhance the ejection motion of the heart or designed for ease of implantation and therefore, introduce aberrant strain patterns during contraction. For example, passive direct compression cardiac devices (e.g., HeartNet (Paracor Surgical Inc.) and C or Cap (Acorn cardiovascular Inc.)) are made of biocompatible mesh or nitinol and placed around the heart as an elastic, compressive reinforcement on the left ventricle to reduce deleterious wall tension during diastole (i.e., restrict end diastolic volume) and to resist shape change of the ventricle during the mechanical cardiac cycle. Similarly, active direct cardiac compression devices are also used to help in ejection of the blood from the left ventricle, thus effectively offload the heart and does not directly modulate the strain pattern, e.g., the rigid cup shaped device of Myo Vad (Myotech LLC). A major disadvantage of this device is that the process of the ejection of the blood inverts the curvature of the heart, which induces aberrant motion and hence an aberrant strain pattern. The inverted curvature leads to a flawed ventricular wall contour and results in regions of stress concentrations in the ventricle, which might lead to aneurysm formation, fibrosis, and impairment of the contractility and compliance of the ventricle. The resulting irregular contour of the endocardial surface of the left ventricle may lead to localized hemostasis or turbulence, which may in turn lead to thrombus formation and possible thromboembolism.
The foregoing problems have been recognized for many years and while numerous solutions have been proposed, none of them adequately address all of the problems.